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Articles by Jared Klarquist
Conserved and Novel Mouse CD8 T Cell Epitopes within SARS-CoV-2 Spike Receptor Binding Domain Protein Identified following Subunit Vaccination
Bennett J. Davenport, Thomas E. Morrison, Ross M. Kedl and Jared Klarquist J Immunol June 1, 2021, 206 (11) 2503-2507; DOI: https://doi.org/10.4049/jimmunol.2100195 Abstract The prior existence of human ACE2 protein–expressing mice used to study SARS-CoV and the rapid development of mouse-adapted virus strains have allowed the study of SARS-CoV-2 in mice, even as we are still learning about its natural pathology in humans.
Conserved and Novel Mouse CD8 T Cell Epitopes within SARS-CoV-2 Spike Receptor Binding Domain Protein Identified following Subunit Vaccination
Bennett J. Davenport, Thomas E. Morrison, Ross M. Kedl and Jared Klarquist J Immunol May 10, 2021, ji2100195; DOI: https://doi.org/10.4049/jimmunol.2100195 Abstract The prior existence of human ACE2 protein–expressing mice used to study SARS-CoV and the rapid development of mouse-adapted virus strains have allowed the study of SARS-CoV-2 in mice, even as we are still learning about its natural pathology in humans.
Clonal expansion of vaccine-elicited T cells is independent of aerobic glycolysis
In contrast to responses against infectious challenge, T cell responses induced via adjuvanted subunit vaccination are dependent on interleukin-27 (IL-27). We show that subunit vaccine–elicited cellular responses are also dependent on IL-15, again in contrast to the infectious response. Early expression of interferon regulatory factor 4 (IRF4) was compromised in either IL-27– or IL-15–deficient environments after vaccination but not infection.
Type I interferon protects CD4 T cells from NK cell killing in a cGVHD model of SLE
Myriad studies have linked type I interferon (IFN) to the pathogenesis of autoimmune diseases, including systemic lupus erythematosus (SLE). While increased levels of type I IFN are found in patients with SLE, and IFN blockade ameliorates disease in most mouse models of lupus, its precise roles in driving SLE pathogenesis remain largely unknown.
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